Current approaches for treating HIV infection are primarily aimed at limiting viral replication or infectivity but do not target latent virus or virally infected cells. As a result of HIV's high mutation rate, drug resistant variants emerge from the latent viral reservoir leading to disease progression in treated patients and infection of other individuals. Several studies have shown that viral escape from CTL responses commonly occurs during the course of the infection. Escape variants may arise through the selection of sequence variations in positions that are important for binding to MHC or in positions that are responsible for interaction between the TCR and the peptide-MHC complex. Circumventing these viral CTL escape mutations is important for eliciting an effective CTL response and for the development of vaccines against HIV-1.
Accordingly, the need exists for therapeutic agents that can effectively target not only the wide-type HIV but also variants that develop during the course of infection.